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ENT workbook > Workbook ENT > Flashcards

Workbook ENT Flashcards

1
Q

Describe the innervation to the external ear.

  1. upper lateral surface
  2. lower lateral and medial
  3. superior medial
  4. external auditory meatus
A
  1. auticulotemporal V3
  2. greater auricular C3
  3. lesser occipital C2/3
  4. auricular branch of vagus
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2
Q

management of external ear laceration

A

closure of skin with sutures after adequate cleaning
clover any exposed cartilage
skin loss may require plastics input

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3
Q

management of ear bites

A

ascertain who bit the ear and work out the commensal organisms.
wound must be left open.
irrigation and antibiotics

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4
Q

management of pinna haematoma

A

disrupt the blood supply to the cartilage by stripping away the overlying perichondrium
this can lead to AVN and cauliflower ear deformity
urgent drainage and pressure dressing to prevent reaccumulation

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5
Q

tympanic membrane perforation

A

pain and possible conductive hearing loss
most heal by themselves- watch and wait with water precautions
if doesn’t heal at 6/12, may benefit from surgery (myringoplasty to repair TM if perforation is causing problems)

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6
Q

Haemotympanum

A

caused by trauma
associated with temporal bone fracture
conductive hearing loss
treated conservatively but follow up for residual hearing loss from damage to ossicles

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7
Q

otitis externa features

A

swimmers ear
bacterial or fungal inflammation of skin lining external canal
caused by regular skin commensals
painful ear discharge, itchy ear, hearing may be muffled

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8
Q

malignant otitis externa features

A

aggressive infection of external ear seen in diabetics and immunosuppressed individuals
infection spreads to bone
chronic ear discharge despite topical treatment, deep seated severe ear pain, cranial nerve palsies (CVII)
10% mortality

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9
Q

management of otitis external

A

topical gentamicin ear drops
swab discharge if resistant
micro suction of pus/debris?
severe infection may need with to keep ear open to deliver gentamicin
antifungals if fungal
malignant OM requires IV abs with extended topical abs to eradicate infection

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10
Q

middle ear epithelium

A

respiratory epithelium- pseudo stratified columnar
continuation of respiratory epithelium
same organisms cause infections- strep pneumonia, haemophilia influenza, moraxella

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11
Q

Features of AOM

A

ear pain caused by increased pressure in tympanic cavity (children may pull their ears)
discharge from tympanic membrane rupture
fever

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12
Q

management of AOM

A

conservative- analgesia
medical- severe cases require abs
recurrent- may require surgery (grommet)

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13
Q

forms of chronic otitis media

A
  1. active mucosal - discharge from middle ear through TM perforation
  2. active squamous - cholesteatoma
  3. inactive mucosal - TM perforation byt no infection/discharge
  4. inactive squamous - retraction pocket
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14
Q

how does mucosal chronic OM develop?

A

from an episode of AOM after rupturing the TM there is failure to heal.

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15
Q

how does active squamous OM develop?

A

keratinised squamous cells are introduced into the middle ear and form a retraction pocket or a perforation

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16
Q

what is active chronic OM associated with?

A

chronic ear discharge
conductive hearing loss
complications- spread of disease into temporal bone or intracranially

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17
Q

management of chronic OM

A

cholesteatoma- surgery to clear cholesteatoma and any affected mastoid bone (mastoidectomy)
mucosal disease- topical abx and aural toilet

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18
Q

what if you are not sure if cholesteatoma is present in a chronically discharging ear?

A

treat medically first, then surgically if doesn’t settle. if in surgery no cholesteatoma is discovered, repair perforation and ensure good ventilation

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19
Q

risks of mastoid surgery

A 
facial nerve palsy 
altered taste from chords tympani palsy 
CSF leak 
tinnitus 
vertigo 
complete hearing loss in that ear
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20
Q

OM with effusion (glue ear) features

A

fluid in middle ear with intact tympanic membrane
related to euschasian tube dysfunction
common in children
in adults, exclude tumour causing obstruction to ET drainage
not painful, but cam before infected (AOM) which is painful
middle ear effusion on otoscope and conductive hearing loss (speech delay, school problems)

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21
Q

how might you investigate OM with effusion?

A
  1. tymponogram - flat type B trade with normal canal volume

2. pure tone audiometry- conductive hearing loss

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22
Q

how is OM with effusion managed?

A

conservative- 3 months
hearing aid
surgery if prolonged and causing significant problems (grommets, ?adenoidectomy)

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23
Q

what is otosclerosis?

A

disease of ossicles where mature bone is replaced by woven bone
symptoms develop as stapes becomes fixed to oval windows
can be environmental or genetic (autosomal dominant)

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24
Q

epidemiology of otosclerosis

A

1-2% of population have it and have symptoms from it
85% will have bilateral disease
F:M 2:1

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25
Q

features of otosclerosis

A

progressive hearing loss
?tinnitus
improved hearing in noisy surroundings at early stages
?family history

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26
Q

examination findings in otosclerosis

A

usually normal examination

rarely schwartze’s sign seen- pink hue to TM

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27
Q

investigation findings in otosclerosis

A
  1. tymponogram- normal type A trace

2. pure tone audiogram- conductive hearing loss, charicteristic Carhart notch at 2kHz

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28
Q

management of otosclerosis

A

hearing aid

stapedectomy

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29
Q

where is the inner ear?

A

petrous part of temporal bone

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30
Q

what does the inner ear consist of?

A

labyrinth of canals: vestibule and semicircular canals, cochlea

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31
Q

outline the structure of the labyrinth

A

membranous labyrinth is filled with endolymph (similar to intracellular fluid). this is surrounded by perilymph (similar to CSF), and contained within the bony labyrinth.
perilymphatic system communicated with subarachnoid space and CSF via the cholerar aqueduct

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32
Q

how is the cchlea (responsible for perception of hearing) different from the rest of the labyrinthine system?

A
  • 2.5 turns around bony core (modiolus)
  • stapes articulates with oval window, moves perilymph, pressure changes are compensated by round window
  • vibrations transmitted through the endolymph to the tectorial membrane
  • movement of tectorial membrane causes movement of hair cells, subsequent depolarisation of neuronal fibres and perception of sound
  • information transmitted via cochlear nerve
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33
Q

where in the cochlea are different sounds detected?

A

low frequency- apex

high frequency- base of cochlea

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34
Q

what makes up the vestibular system?

A

semicircular canals (three, at 90 degrees to each other)
utricle
saccule

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35
Q

functions of vestibular system

A

Utricle- hairs point up to detect horizontal movement
saccule- hairs on side to detect vertical movement
semicircular canals- detect rotatory movement

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36
Q

what contributes to good balance?

A

vestibular system
proprioception
vision

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37
Q

what is vertigo?

A

hallucination of movement

associated with vestibular system problems

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38
Q

central causes of vertigo

A 
stroke
migrane 
neoplasm 
demyelination e.g. MS 
Drugs
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39
Q

peripheral causes of vertigo

A

BPPV
Menieres
Vestibular Neuronitis

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40
Q

BPPV

  1. features
  2. pathophysiology
A
  1. vertigo with head movements lasting seconds-minutes, very distressing
  2. otoliths (crystals) in semicircular canals (usually posterior) cause abnormal stimulation of hair cells
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41
Q

how is BPPV

  1. diagnosed
  2. treated
A
  1. Dix-Hallpike test

2. Epley manoeuvre

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42
Q

pathophysiology of Menieres disease

A

endolymphatic hydrops (increased fluid in endolympthatic compartment)

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43
Q

clinical features of Menieres

A

tinnitus in affected ear
episodic vertigo lasting minutes- hours with N&V
fluctuating sensorineural hearing loss which over time becomes permanent
aural fullness

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44
Q

investigations for sudden onset sensorineural hearing loss

A

pure tone audiogram

MRI scan to exclude lesion along central auditory pathway eg acoustic neuroma

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45
Q

management of sudden onset sensorineural hearing loss

A

steroids - usually oral, can be injected into middle ear
antivirals
rarely hyperbaric oxygen or carbogen

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46
Q

which hearing loss requires urgent treatment?

A

sudden onset sensorineural

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47
Q

which tuning forks are used?

A

256 or 512Hz

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48
Q

Weber test

A

on forehead
localises to ear with conductive hearing loss/without sensorineural hearing loss
(because in conductive hearing loss, background noise is cancelled out and bone conduction is normal)

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49
Q

Rinne test

A

placed on mastoid bone until can’t hear. then, placed against external auditory meatus.
conducted to cochlea via temporal bone
can still hear it = positive result = sensorineural and normal (AC>BC)
can’t hear it= negative result= conductive hearing loss (BC>AC)

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50
Q

Pure tone audiogram

A

tests hearing thresh points at different frequencies
can be used from age 4
quietest tone which can be reliably heard by each ear at different frequencies is plotted
air conduction and bone conduction thresholds tested

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51
Q

pure tone audigraph

A

frequency in Hz on x axis
descend on y axis in decibels (the quieter the noise, the higher the line and better hearing. anything above 20dB is normal)

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52
Q

Menieres disease course

A

initially- well between attacks
progresses
feel generally unsteady due to reduced vestibular Winston and progressive sensorineural hearing loss
disease often burns out- no more acute vertigo, but reduced heating and generally unbalanced
is the vestibular system of the other ear is working well, this can compensate for bad ear

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53
Q

dietary management of Menieres

A

reduce salt, chocolate, alcohol, caffeine, Chinese food

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54
Q

medical management of Menieres

A

Thiazide diuretic
Betahistine
vestibular sedatives eg prochlorperazine for acute attacks

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55
Q

surgical management options for Menieres

A 
Grommets
dexamethasone middle ear injection 
Endolymphatic sac decompression 
vestibular destruction using middle ear injection of gentamicin 
surgical labyrinthectomy (rare)
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56
Q

What is vestibular neuritis

A

inflammation of middle ear
severe incapacitating vertigo lasting several days with N&V
during attack- horizontal nystagmus but otherise normal neurological examination

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57
Q

treatment of vestibular neuritis

A

symptomatic:
vestibular sedatives during acute episode
IV fluids

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58
Q

prognosis of vestibular neuritis

A

often long term vestibular deficit after the acute episode which can lead to generalised unsteadiness for a number of weeks

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59
Q

management of long term complications of vestibular neuritis

A

if patients are suffering from a long term vestibular dysfunction in one ear, may be helped by vestibular rehabilitation exercises such as the Cawthorne-Cooksey exercises. after the acute attacks, patients should not take vestibular suppressants as this delays recovery.

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60
Q

sudden onset sensorineural hearing loss

A

otological emergency

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61
Q

prognosis for sudden onset sensorineural hearing loss

A

1/3 recovery to normal
1/3 some recovery
1/3 no recovery

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62
Q

how is bone conduction tested during PTA

A

tone played through conductor placed over mastoid bone.
sound passes through bone straight into cochlea, bypassing conductive hearing system, so it approximates sensorineural hearing.
some sound is conducted to the other ear, so if there are any disprecancies between two ears, the other ear will need to be masked.

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63
Q

features of conductive hearing loss

A

impedance to hearing in middle or external ear
eg wax, OM with effusion
PTA will show normal BC and reduced AC (an air bone gap)

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64
Q

features of sensorineural hearing loss

A

problem in cochlea-auditory cortex of the brain
asymmetrical sensorineural hearing loss should be investigated with an MRI scan looking for lesions along the pathway eg acoustic neuroma (vestibular schwannoma)
PTA will have reduced AB and reduced BC- no air bone gap

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65
Q

old age hearing loss

A

bilateral
sensorineural
presbycusis
(may also be components of conductive)

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66
Q

tymponogram

A

simple test which measures compliance of TM and gives information about TM, middle ear and ET function.
probe is inserted into external ear canal
can be done at any age, takes few seconds, and requires minimal cooperation from patient

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67
Q

reading from tymponogram

A

compliance in ml (y axis) vs pressure (x axis in daPascals)
compliance of TM measured with varying amounts of pressure in external canal which is sealed by probe.
compliance peaks when pressure in canal equals that of middle ear

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68
Q

type A tymponogram trace

A

normal result

peak at 0kPa

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69
Q

type B tymponogram trace

A

flat tracing
suggests middle ear effusion or perforation
by look at the canal volume reading on the side of the tymponogram you can differentiate between effusion and perforation. effusion has a normal canal volume (1ml in adults) whereas in perforation the volume is much larger

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70
Q

type C tymponogram trace

A

peak of tracing has a negative pressure

suggests ET dysfunction

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71
Q

Little’s area

A

also known as Kiesselbach’s plexus
highly vascular area on nasal septum
receives contribution from branches of external carotid and internal carotid arteries

72
Q

Epistaxis- what is it

A

bleeding from nose

73
Q

local causes of epistaxis

A 
idiopathic 85% 
traumatic 
iatrogenic 
foreign body 
inflammatory- rhinitis, polyps 
neoplasm
74
Q

systemic causes of epistaxis

A

HTN
coagulopathies
vasculopathies
hereditary haemorrhage telangiectasia/osler-weber-rendu disease

75
Q

management of epistaxis

A 
ABC 
pinch soft part of nose 
head forward 
spit out blood 
cautery (silver nitrate or bipolar diathermy) 
nasal packing if cautery fails
76
Q

detail on epistaxis cautery

A

silver nitrate or bipolar diathermy
if anterior bleed- with anterior rhinoscopy
if posterior bleed- with rigid endoscope
topical adrenaline may help control bleeding

77
Q

surgical management of epistaxis

A

if nasal packing fails, vessels can be surgically ligated or radiological embossed:
sphenopalatine
anterior ethmoid (cannot be embossed because it comes form international carotid)
external carotid

78
Q

complications of nasal fracture

A

septal haematoma

CSF leak associated with skull base fracture

79
Q

management of nasal trauma

A

ABC
examine for septal haematoma
no XR required
consider manipulation under anaesthetic within 2 weeks of injury (LA/GA)

80
Q

lamina papyracea

A

forms medial wall of orbit

81
Q

what drains into these structures?

  1. sphenoid-ethmoidal rescues
  2. superior meatus
  3. middle meatus
  4. inferior meatus
A
  1. sphenoid sinus
  2. posterior ethmoid cels
  3. frontal, maxillary and anterior ethmoid cells
  4. nasolacrimal duct
82
Q

complications of sinus surgery

A
  1. damage to orbit- lies lateral to ethmoid sinus and superior to maxillary sinus (severe cases can cause loss of sight)
  2. anterior skull base- lies just above the sphenoid and ethmoid sinuses and can be breached during surgery which can cause CSF leak and brain damage
83
Q

complications of rhino sinusitis

A
  1. can spread to orbit to cause peri orbital sinusitis which can be sight threatening
  2. from frontal sinus can spread intracranially causing meningitis and intracranial abscesses
84
Q

define rhino sinusitis

A

inflammation of nose and paranasal sinuses characterised by two or more symptoms, one of which could be:

  • nasal blockage/obstruction/congestion/discharge
  • anterior/posterior postnasal drip
  • facial pain/pressure
  • reduced sense of smell
85
Q

other features of rhinosinusitis

A
  • endoscopic signs of polyps, mucopurulent discharge or oedema in middle meatus
  • CT changes- mucosal changed within the osteomatal complex or sinuses
86
Q

how is rhino sinusitis classified?

A

Acute: <12/52, complete resolution of symptoms. viral or on viral
Chronic: 12/52, without complete resolution of symptoms
with or without polyps

87
Q

ARS

A

Viral ARS (common cold) is usually caused by rhinovirus or influenza virus with resolution within 5 days
non viral ARS is considered if >5/7, usually bacterial: H influenzae, Moraxella catarrhalis.
allergy and ciliary impairment predispose to ARS

88
Q

management of ARS

A

analgesia
nasal decongestant
if >5/7, consider nasal steroids and oral abs

89
Q

CRS predisposing factors

A

Allergy, Infection, Ciliary impairment (CF, nasal polyps), Anatomical (septal deviation, abnormal unicante process leading to narrow infundibulum and occlusion of osteomeatal couples), immunocompromised, aspirin hypersensitivity, Atmospheric irritants (smoking, dust, fumes), hormonal (pregnancy, hypothyroidism), trauma (oroantral fistula, nasal sinus fracture), foreign body in nose or sinus, swimming

90
Q

CRS in pregnancy

A

oestrogen and progesterone increase mucosal vascularity and predispose to CRS

91
Q

Nasal polyps

A

inflammatory mass
normally bilateral
biopsy if unilateral or worrying signs or findings

92
Q

investigating CRS

A 
skin prick if allergy suspected 
CT sinuses (if surgery is planned, if atypical features- not good for diagnosis as many patients will have sinus changes even if asymptomatic)
93
Q

management of CRS

A

conservative- avoid allergens, nasal douching
medical- antihistamines, topical nasal steroid, one week oral steroids if severe, oral antibiotics
surgical- nasal polypectomy (very high rate of recurrence), functional endoscopic sinus surgery to improve drainage/ventilation, septoplasty, reduction of inferior turbinates

94
Q

what is allergic rhinitis

A

an IgE mediated type 1 hypersensitivity reaction in the mucus membranes of nasal airways. affects 30% western population. associated with asthma. seasonal or perennial. commonest allergens: pollens, moulds, house dust mites, animal epithelia

95
Q

how is allergic rhinitis classified?

A

allergic rhinitis according to its impact on asthma (ARIA) and other health issues. based on duration and severity

96
Q

duration of allergic rhinitis.

A

intermitent <4 days a week, less than 4 weeks

persistent >4 days a week, more than 4 weeks

97
Q

severity of symptoms of allergic rhinitis

A

mild- normal daily activities and sleep

moderate to severe- impairment of daily activities and sleep, troublesome symptoms

98
Q

pathophysiology of allergic rhinitis

A

synthesis and release of arachidonic acid metabolites (prostaglandin D and leukotrienes) and mast cell degranulation. in turn increased capillary permeability leading to congestion, odedema, rhinorrhoes, sneezing and irritation

99
Q

investigations for allergic rhinitis

A

SPT for specific antigen

RAST blood test if SPT not possible

100
Q

management of allergic rhinitis

A

conservative - allergen avoidance, nasal douching
medical- antihistamines, topical nasal steroids
immunotherapy

101
Q

how does periorbital sinusitis develop?

A

from direst spread of pus from the ethmoid sinus, or from thrombophlebitis of mucosal vessels in any of the sinuses

102
Q

symptoms of periorbital sinusitis

A

pain followed by oedema of the eyelids
is orbital abscess develops- eye will become proposed and eye movements will be reduced.
risk of blindness as a result of tension and septic necrosis of the optic nerve.
colour blindness is an early sign

103
Q

investigating periorbital sinusitis

A

CT scan will confirm the collection and the extent of the disease

104
Q

treatment of periorbital sinusitis

A

IV abs
nasal decongestants
urgent surgical drainage if abscess

105
Q

boundaries of anterior triangle of the neck

  1. medial
  2. lateral
  3. superior
A
  1. midline of neck
  2. anterior boarder of SCM
  3. lower boarder of the mandible
106
Q

posterior triangle of neck boundaries

  1. anterior
  2. posterior
  3. base
A
  1. posterior boarder of SCM
  2. anterior edge of trapezius
  3. middle third of clavicle
107
Q

where may a retropharyngeal abscess form?

A

anterior to the prevertebral fascia, behind the pharynx

is the retropharyngeal space. extends from base of skull to mediastinum.

108
Q

clinical features of a retropharyngeal abscess

A

young child after URTI
neck held rigid and upright with reluctance to move
systematically unwell
airway compromise
dysphagia/odynophagia
widening of retropharyngeal space on lateral X ray
associated mortality due to airway problems and mediastinitis

109
Q

investigations for a retropharyngeal abscess

A

CT neck

110
Q

management of a retropharyngeal abscess

A

secure airway if any concerns
IV abs
surgery- I&D

111
Q

what is Ludwigs angina

A

infection of the space between the floor of the mouth and mylohyoid, commonly associated with dental infection

112
Q

clinical features of Ludwigs angina

A 
swelling of the floor of the mouth 
painful mouth 
protruding tongue 
airway compromise 
drooling
113
Q

investigations for Ludwig’s andgina

A

CT neck

OPG

114
Q

management of Ludwigs angina

A

secure airway if concerns
IV abs
surgery to drain any collection

115
Q

where is a parapharyngeal abscess?

A

posteriolateral to oropharynx and nasopharynx which is divided by the styloid process.

116
Q

how does a parapharyngeal abscess present?

A

similar to peritonsillar abscess or quinsy
febrile illness, odynophagia, trismus, reduced neck movement, swelling in the neck and around the upper part of the SCM.
parapharyngeal space contains the carotid sheath- risk of severe complications in this area

117
Q

management of parapharyngeal abscess

A

secure airway if concerned
IV abs
surgical drainage

118
Q

epiglottitis causes

A

haemophilus influenza

incidence reduced by HIB vaccine

119
Q

presentation of epiglottis

A

stridor
drooling
pyrexia
rapidly progressive

120
Q

management of epiglottis

A 
secure the airway- do not examine 
keep calm 
if possible, take child to theatre and intubate by paediatric anaesthetist with an ENT surgeon on standby to do a surgical airway if intubation is not possible. 
if transfer to theatre not safe, intubate in A&E 
IV abs (normally respond within couple days and then extubated)
121
Q 
Neck lumps 
where may these be found? 
1. parotid neoplasm 
2. jugulodigastric 
3. submandibular gland 
4. carotid body tumour or aneurysm
A
  1. anterior to ear
  2. angle of mandible
  3. inferior boarder of mandible
  4. at bifurcation of common carotid artery
122
Q

neck lumps- where may these be found?

  1. thyroglossal cyst
  2. branchial cyst
  3. thyroid nodule
  4. Virchows node
A
  1. in midline between hyoid bone and thyroid gland
  2. anterior boarder of SCM
  3. at level of thyroid
  4. supraclavicular dossa node may represent metastasis
123
Q

where is the oral cavity?

A

lips - posterior soft palate

124
Q

whee is the nasopharynx?

A

base of skull to level of soft palate

contains adenoids and ET opening

125
Q

where is the oropharynx?

A

from soft palate to superior boarder of epiglottis

contains palatine tonsils and anterior and posterior tonsillar pillars

126
Q

where is the hypotharynx?

A

from superior boarder of epiglottis to inferior boarder of cricoid cartilage, posterior to the larynx

127
Q

muscles of pharynx

A

a circular layer formed by superior, middle and inferior constrictors, and the cricopharynxgeus

128
Q

Killian’s dehiscence

A

area deficient in muscle between the inferior constrictor and the cricopharyngeous
site of pharyngeal pouches

129
Q

how fo pharyngeal pouches present?

A

dysphagia, delayed regurgitation of food and sometimes recurrent chest infections due to aspirated food

130
Q

which muscles cause elevation and depression of pharynx?

A

stylopharyngeous
salpingopharyngeous
palatopharyngeous

131
Q

what is snoring a sign of?

A

partial obstruction of the upper airway during sleep (nose-larynx)

132
Q

what is the pathophysiology of OSA?

A

complete obstruction of upper airway during sleep requires patient to wake up and reposition to open up the airway. apnoeas result in poor nights sleep and strain on caridovascular system.

133
Q

main causes of OSA

A

obesity in adults

adenotonsillar hypertrophy in children

134
Q

investigations to consider in OSA

A 
BMU 
TFT for hypo 
CXR for obstructive lung disease 
ECG for signs of RV failure 
sleep study
135
Q

management of OSA

A

weight loss
CPAP
?mandubular repositioning devices
?adenotonsilectomy in children (rare in adults)

136
Q

bacterial causes of tonsillitis

A 
B haemolytic strep 
staphylococci 
strep pneumonia 
haemophilus influenza 
E coli
137
Q

viral causes of tonsillitis

A

adenovirus
rhinovirus
enterovirus
EBV

138
Q

amoxicillin in tonsilitis

A

should be avoided

will cause maculopapular rash in EBV

139
Q

EBV advice

A

avoid contact sport for 2-3 months due to hepatosplenomegaly

140
Q

quinsy

A

peritonsillar abscess
sore throat localised to one side and a ‘hot potato’ voice
amendable to drainage under LA

141
Q

histopathology of H&N cancers

A

90% are SCC

142
Q

which ethnicity has a higher risk of nasopharyngeal malignancy?

A

Chinese

143
Q

when is histology/cytology of neck lumps not required?

A

proven H&N SCC (assume any LN are due to this- CT)

144
Q

why should you do FNA before core biopsy

A

core biopsy can lead to tumour seeding therefor FNA first, exclude SCC, core biopsy to diagnose TB or lymphoma

145
Q

what is a goitre?

A

an enlarged thyroid gland

146
Q

what is a thyroid nodule?

A

an abnormal mass in the thyroid

147
Q

investigation of thyroid nodules

A

check that they are not functioning leading to hyperthyroidism and that they are not neoplastic

148
Q

complications of large goitres?

A

can cause compression leading to airway obstruction and dysphagia

149
Q

blood supply and drainage to thyroid gland

A

supply- superior and inferior thyroid arteries

drainage- superior, middle and inferior thyroid veins

150
Q

where is the RLN at the thyroid?

A

intimately associates with the thyroid glad: run in the tracheooesophygeal groove therefore at risk during surgery

151
Q

RLN function

A

supply the muscles of the larynx except cricothyroid and sensation below vocal cords

152
Q

injury of RLN

A

vocal cord palsy- hoarseness, upper airway obstruction in both damaged

153
Q

assessment of thyroid nodules

A

FNA
if there is any diagnostic doubt, hemithyroidectomy for definitive histology
lumpectomies are not done because if it is malignant the margins would likely not be enough and scarring would make further surgeries difficult
FNA are not accurate for differentiating follicular carcinoma from follicular adenoma and in these cases hemithyroidectomy should be done

154
Q

non-neoplastic thyroid nodules

A

single nodule- colloid, cystic

multi nodular goitre- common, typical features on USS and no need for FNA. any dominant nodule however should have FNA

155
Q

thyroid neoplasms

A

benign- usually follicular adenoma
malignant:
papillary adenocarcinoma (70%, younger pt or history of neck radiation)
follicular carcinoma- 20% (preponderance to met to bones and lung)

156
Q

rare thyroid malignant neoplasms

A

medullary carcinoma 5%- neoplasm of calcitonin regulating C cells, frequently seen in MEN syndromes
anaplastic carcinoma 5%- typically in older patients, poor prognosis (weeks to months)

157
Q

management of non neoplastic thyroid nodules

A

usually conservative unless diagnostic uncertainty
surgery: for compressive symptoms, cosmoses or patient preference
(hemithyroidectomy is best because total thyroidectomy requires lifelong thyroxine)

158
Q

management of neoplastic thyroid nodules

A

adenomas require no further treatment after diagnostic hemithyroidectomy
carcinoma- surgery (total for papillary, follicular and medullary, anaplastic disease is usually too advanced for surgery)
radio iodine therapy for papillary and follicular after surgery

159
Q

complications of thyroid surgery

A

post op haemorrhage
airway obstruction (secondary to haemorrhage, secondary to bilateral vocal cord palsy)
vocal cord palsy
hypocalcaemia

160
Q

parotid gland anatomy

A

serous salivary gland located anterior to pinna and lateral to the ramps of the mandible
split into deep and superficial lobes by the facial nerve which passes through it
majority is superficial
facial nerve palsy is a serious complication of parotid cancer or surgery

161
Q

parotid duct anatomy

A

opens opposite the second upper molar tooth after piercing the buccinator muscle and buccal mucosa

162
Q

salivary gland neoplasms

A

80% in parotid
80% of parotid neoplasms are benign
80% of benign parotid neoplasms are pleomorphic adenomas

163
Q

salivary gland infections

A

9X more common in submandibular than parotid

164
Q

submandibular gland anatomy

A

located inferior to the mandible and superior to the digastric
its duct opens into the mouth close to the frenulum of the tongue
hypoglossal and lingual nerves run medial to the gland and are at risk during surgery
produces mixed mucous and serous secretions

165
Q

sublingual gland secretions

A

entirely mucous

located at the floor of the mouth

166
Q

submandibular gland neoplasms

A

50% are malignant

167
Q

sublingual gland neoplasms

A

80% are malignant

168
Q

submandibular abscesses

A

can follow sialolithiasis or sialadenitis

169
Q

acute sialadenitis

A

can be viral or bacteria
bacterial usually staphylococcal (dehydrated or immunocompromised)
viral: paramyxovirus (mumps), coxsackievirus, echovirus, HIV

170
Q

chronic sialadenitis

A

rare, seen in TB, sarcoidosis, HIV and syphilis

171
Q

sialolithiasis

A

stones in salivary duct
cause obstruction and subsequently lead to pain and swelling which is worse during meals
9X more common in submandibular than parotid

172
Q

investigations in suspected sialolithiasis

A

USS

or sialogram

173
Q

management of sialolithiasis

A

most settle with conservative- analgesic, hydration, sialogogues
endoscopy
radiological removal
surgery (remove palpable stones or salivary gland)

174
Q

complications of sialolithiasis

A

sialadenitis

abscess formation

175
Q

Sjorgens syndrome features

A 
Autoimmune disease causing lymphocytic infiltration into ductal tissue of secretory glands 
dry eyes 
dry mouth 
enlarged salivary gland 
increased lymphoma risk
176
Q

causes of Sjorgens

A

primary- Xerostomia and Xerophthalmia without connective tissue abnormality
secondary- with connective tissue disease, eg rheumatoid arthritis

177
Q

diagnosis of sjorgens

A

history, examination, some specific antibodies, biopsy of minor salivary glands on the inner lip

ENT workbook (1 decks)

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